SrasV1, PascalFrancis, Curation, bibRecord, 000914

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Identifieur interne : 000914 ( PascalFrancis/Curation ); précédent : 000913; suivant : 000915

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Auteurs : Martial Jaume [Hong Kong] ; Ming S. Yip [Hong Kong] ; Chung Y. Cheung [Hong Kong] ; Hiu L. Leung [Hong Kong] ; Ping H. Li [Hong Kong] ; Francois Kien [Hong Kong] ; Isabelle Dutry [Hong Kong] ; Benoit Callendret [France] ; Nicolas Escriou [France] ; Ralf Altmeyer [Hong Kong] ; Beatrice Nal [Hong Kong] ; Marc Daëron [France] ; Roberto Bruzzone [Hong Kong, France] ; J. S. Malik Peiris [Hong Kong]

Source :

Journal of virology [ 0022-538X ] ; 2011.

RBID : Pascal:12-0111133

Descripteurs français

Pascal (Inist)
- Coronavirus, Homme, Anticorps, Cysteine endopeptidases, Récepteur FcγR, Syndrome respiratoire aigu sévère.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Antibody, Coronavirus, Cysteine endopeptidases, FcγR receptor, Human, Severe acute respiratory syndrome.

Abstract

Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.

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Le document en format XML

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<author><name sortKey="Nal, Beatrice" sort="Nal, Beatrice" uniqKey="Nal B" first="Beatrice" last="Nal">Beatrice Nal</name>
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<author><name sortKey="Daeron, Marc" sort="Daeron, Marc" uniqKey="Daeron M" first="Marc" last="Daëron">Marc Daëron</name>
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<author><name sortKey="Malik Peiris, J S" sort="Malik Peiris, J S" uniqKey="Malik Peiris J" first="J. S." last="Malik Peiris">J. S. Malik Peiris</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway</title>
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<series><title level="j" type="main">Journal of virology</title>
<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
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<front><div type="abstract" xml:lang="en">Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway</s1>
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<fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0>
<s5>13</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>16</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>086</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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   |wiki=    Sante
   |area=    SrasV1
   |flux=    PascalFrancis
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   |clé=     Pascal:12-0111133
   |texte=   Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway
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Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

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